Nicotine reduces the binding of [3H]MK-801 to brain membranes, but not via the stimulation of high-affinity nicotinic receptors.
Nicotine (10 and 100 microM) inhibited [3H]MK-801 binding to rat cerebral cortical membranes and this effect was not blocked by dihydro-beta-erythroidine, (+)-tubocurarine or mecamylamine. Cytisine, muscarine mecamylamine and (+)-tubocurarine also inhibited [3H]MK-801 binding. Neither raising the MK-801 concentration, nor the addition of n-methyl-D-aspartate (NMDA) receptor agonists altered the effects of nicotine. Hence this response is not mediated via high-affinity nicotinic receptor stimulation, competition for MK-801 binding sites or require NMDA receptor activation.
Court
J A
JA
MRC Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne U.K.
Piggott
M A
MA
Perry
E K
EK
D000818:Animals; D000927:Anticonvulsants / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D016291:Dizocilpine Maleate / Q000378:metabolism*; D007700:Kinetics; D009538:Nicotine / Q000494:pharmacology*; D010277:Parasympathomimetics / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011978:Receptors, Nicotinic / Q000502:physiology*
D000927:Anticonvulsants; D002800:Cholinesterase Inhibitors; D010277:Parasympathomimetics; D011978:Receptors, Nicotinic; D016291:Dizocilpine Maleate; D009538:Nicotine